CASE A
A 50-year-old man with a history of chronic obstructive pulmonary disease and hypertension was found unresponsive. ADC, apparent diffusion coefficient; Ax, axial; CT, computed tomography; DWI, diffusion-weighted imaging; FLAIR, fluid attenuated inversion recovery.

CASE B
A 67-year-old man presenting with ataxia, rapidly progressive deterioration in mental status, and myoclonus. ADC, apparent diffusion coefficient; Ax, axial; DWI, diffusion-weighted imaging; FLAIR, fluid attenuated inversion recovery.

CASE C
An 11-year-old boy with chronic progressive neurologic symptoms since the age of 9 years. ADC, apparent diffusion coefficient; Ax, axial; DWI, diffusion-weighted imaging; FLAIR, fluid attenuated inversion recovery.

CASE D
A 72-year-old woman with a history of coronary artery bypass grafting who was unable to be aroused in the morning. ADC, apparent diffusion coefficient; Ax, axial; Cor, coronal; CT, computed tomography; CTA, CT angiography; DWI, diffusion-weighted imaging; FLAIR, fluid attenuated inversion recovery; Recon, reconstruction.

DESCRIPTION OF FINDINGS

  • Case A: Uniform, bilateral restricted diffusion is noted involving the caudate nuclei, putamina, and cerebral cortex. These structures are hyperintense on FLAIR and T2-weighted images and hypodense on noncontrast CT. Swelling of the ischemic structures also is noted.

  • Case B: Patchy, nonuniform areas of restricted diffusion and FLAIR hyperintensity involve the cerebral cortex (including the cingulate gyri), as well as the caudate nuclei and putamina. Bilateral symmetric involvement of the thalamic pulvinar and dorsomedial thalamic nuclei are present (consistent with a “hockey stick” sign).

  • Case C: Prominent, symmetric, bilateral globus pallidus central FLAIR and T2 hyperintensity is present with surrounding hypointensity consistent with the “eye of the tiger” sign. The lesions have central hypointensity on T1-weighted images.

  • Case D: Bilateral anterior thalamic CT hypodensity and restricted diffusion consistent with bilateral thalamic infarction is present. The infarctions are mildly hyperintense on FLAIR and T2-weighted images. Coronal CT angiography reconstruction demonstrates a focal unilateral occlusion of the left P1 segment at the expected site of thalamoperforators.

Diagnosis

Case A

Hypoxic-ischemic encephalopathy (HIE)

Case B

Creutzfeldt-Jakob disease (CJD)

Case C

Neurodegeneration with brain iron accumulation (NBIA) (formerly Hallervorden-Spatz disease) resulting from PANK2 mutation

Case D

Bilateral thalamic infarcts resulting from occlusion of the artery of Percheron

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